Interphase cytogenetic analysis of cervical intraepithelial neoplasia.
The aim of this study was to detect numerical chromosomal aberrations that may be involved in the progression of cervical intraepithelial neoplasia (CIN) toward cervical carcinoma. Therefore, cervical lesions (five CIN 1, seven CIN 2, six CIN 3, six invasive carcinomas, and six normal samples) were studied by in situ hybridization (ISH) on serial 3-microm-thick paraffin tissue sections, using a panel of eight centromeric DNA probes for chromosomes 1, 3, 6, 7, 8, 11, 17, and X. An estimation of the percentage of dysplastic epithelium with abnormal ISH signals per nucleus was made. Chromosome aneusomy could be detected in all persisting and high-grade CIN lesions and invasive carcinomas. In most cases, when one of the chromosomes showed aneusomy then all studied chromosomes showed numerical changes. Interestingly, the abnormal ISH signals were found only in a varying part of the morphologically dysplastic epithelium, the remainder showing no such changes. In aneuploid regions of the CIN 1 lesions the mean chromosome index for all chromosomes was 1.97+/-0.03 with a range of 1.92 to 2.00. The chromosome index ratios of chromosomes 1, 7, and X showed a significant positive correlation with CIN grade (r > or = 0.74; P < or = 0.006). It is concluded that chromosome aneusomy of chromosomes 1, 7, and X may be involved in the progression of CIN lesions.
Bulten
J
J
Institute of Pathology, University Hospital Nijmegen, The Netherlands.
Poddighe
P J
PJ
Robben
J C
JC
Gemmink
J H
JH
de Wilde
P C
PC
Hanselaar
A G
AG
D000328:Adult; D000368:Aged; D000782:Aneuploidy; D002869:Chromosome Aberrations / Q000235:genetics; D003582:Cytogenetics / Q000379:methods*; D005260:Female; D006801:Humans; D017403:In Situ Hybridization; D007399:Interphase / Q000502:physiology*; D008875:Middle Aged; D009361:Neoplasm Invasiveness / Q000235:genetics; D012189:Retrospective Studies; D002583:Uterine Cervical Neoplasms / Q000235:genetics* / Q000473:pathology; D002578:Uterine Cervical Dysplasia / Q000235:genetics* / Q000473:pathology